. Indeed, T cells that lack lamins or have disconnected LINC–lamin complexes have impaired activation and proliferation. Similar to many mechanosensitive proteins in immune cells, A-type lamins together with the LINC complex have the ability to bridge actin remodelling and transcription in the nucleus, therefore hinting to their indispensable role in immune mechanotransduction.
co-localization with some Toll-like receptors . Force-triggered opening of transient receptor potential vanilloid type 4 and leads to Calevels induce actin polymerization and activate Rho GTPase, boosting phagocytosis. Concurrently, F-actin formation depletes G-actin availability, and without G-actin to bind to, myocardin-related transcription factor A is shuttled into the nucleus where it forms a complex with serum response factor .
enables transcription of immune effector genes, such as those encoding interleukin-6 and CXC-chemokine ligand 9 , generally skewing the cell towards an enhanced inflammatory phenotype. Caalso enforces TLR signalling by promoting the expression and activation of endothelin 1 and NF-κB. EDN1 stabilizes hypoxia-inducible factor 1α , promoting TLR-induced HIF1α accumulation. Active NF-κB and HIF1α translocate to the nucleus and drive metabolic and inflammatory gene expression.
also activates histone deacetylases to further induce inflammatory cytokine output. Dashed lines represent pathways where there are still major gaps in understanding the transduction mechanisms, and solid lines depict more well-described pathways. Linker of nucleoskeleton and cytoskeleton complex modulation of immune activation has been shown in adaptive cells only, but we hypothesize it also plays a role in innate immune cell regulation.
physorg_com Via classical or quantum mechanics?
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